Pathogenesis of Trypanosoma brucei infection in deer mice (Peromyscus maniculatus). Ultrastructural pathology of the spleen, liver, heart, and kidney.

Abstract

Trypanosoma brucei EATRO 110 infection of the deer mice (Peromyscus maniculatus) produced moderate to marked lesions in the spleen, liver, heart, and kidney seven to ten weeks after infection. Splenic lesions consisted of marked splenomegaly, with infected spleens weighing 25.9 times control spleens. Transmission electron microscopy of the sinuses and Billroth's cords of the splenic red pulp demonstrated an increased cellularity with greater contact between cells due partly to proliferation of macrophages, transformed lymphocytes and plasma cells and partly to accelerated erythropoiesis with increases in the numbers of rubricytes and reticulocytes. Erythrocytes also were present in large numbers, and erythroclasis was accelerated. Hepatic lesions consisted of necrosis of few hepatocytes, proliferation and hypertrophy of Kupffer's cells which exhibited increased phagocytosis--particularly of erythrocytes, as well as perivascular cuffs consisting of lymphocytes, plasma cells and macrophages. Myocarditis was marked and was characterized by degeneration of myocardial fibers with decreases in mitochondrial size and myofibril contents and fragmentation of some degenerating fibers, and was accompanied by accumulation of inflammatory cells including lymphocytes, transformed lymphocytes, plasma cells, and macrophages between the myocardial fibers. Renal lesions consisted of severe glomerulonephritis characterized by deposition of electron dense material along the basement membrane and in the mesangium of the glomerular tufts, and less frequently beneath the basement membrane and visceral epithelium of the Bowman's capsule and within the peritubular vessels. Neutrophils with fewer macrophages and lymphocytes invaded the glomeruli.(ABSTRACT TRUNCATED AT 250 WORDS)